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. 2020 Nov:145:111716.
doi: 10.1016/j.fct.2020.111716. Epub 2020 Sep 3.

Paternal bisphenol A exposure in mice impairs glucose tolerance in female offspring

Cetewayo S Rashid  1 , Amita Bansal  2 , Clementina Mesaros  3 , Marisa S Bartolomei  4 , Rebecca A Simmons  5
Affiliations

Paternal bisphenol A exposure in mice impairs glucose tolerance in female offspring

Cetewayo S Rashid et al. Food Chem Toxicol. 2020 Nov.

Abstract

Humans are ubiquitously exposed bisphenol A (BPA), and epidemiological studies show a positive association between BPA exposure and diabetes risk, but the impact of parental exposure on offspring diabetes risk in humans is unknown. Our previous studies in mice show disruption of metabolic health upon maternal BPA exposure. The current study was undertaken to determine whether exposure in fathers causes adverse metabolic consequences in offspring. Male C57BL/6 J mice were exposed to BPA in the diet beginning at 5 weeks of age resulting in the following dietary exposure groups: Control (0 μg/kg/day), Lower BPA (10 μg/kg/day) and Upper BPA (10 mg/kg/day). After 12 weeks of dietary exposure, males were mated to control females. Mothers and offspring were maintained on the control diet. Post-pubertal paternal BPA exposure did not affect offspring body weight, body composition or glucose tolerance. However, when fathers were exposed to BPA during gestation and lactation, their female offspring displayed impaired glucose tolerance in the absence of compromised in vivo insulin sensitivity or reduced ex vivo glucose-stimulated insulin secretion. Male offspring exhibited normal glucose tolerance. Taken together, these studies show there is an early window of susceptibility in which paternal BPA exposure can cause sex-specific impairments in glucose homeostasis.

Keywords: Bisphenol a; Body composition; Developmental programming; Diabetes; Glucose tolerance; Paternal.

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Conflict of interest statement

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Figure 1.
Figure 1.
Metabolic phenotyping of male mice exposed post-puberty to dietary BPA. (A) Body weight of sires for the first 4 months on the BPA-containing diets. (B) Fasting serum BPA levels 4 months on respective diets. Glucose tolerance (C), AUC (D), and insulin tolerance (E) at 6 months of age. Glucose tolerance (F) and AUC (G) at 1 year of age. * p<0.05 compared to controls.
Figure 2.
Figure 2.
Metabolic phenotype of offspring from sires exposed to BPA post-puberty. Male offspring body weight (A), body composition (B), and glucose tolerance (C) at 4 months of age. Female offspring body weight (D), body composition (E), and glucose tolerance (F) at 4 months of age.
Figure 3.
Figure 3.
Metabolic phenotyping of male offspring from sires developmentally exposed to BPA. Body weight (A), body composition (B), and glucose tolerance (C) at 4 months of age. Data represents two independent cohorts.
Figure 4.
Figure 4.
Metabolic phenotyping of female offspring from sires developmentally exposed to BPA. Body weight (A), body composition (B), and glucose tolerance with AUC (C and D) at 4 months. Glucose tolerance with AUC (E and F), insulin tolerance (G), and ex vivo islet perifusion with AUC (H and I) at 7 months of age. * p<0.05 Lower BPA vs Control; ## p<0.01 Upper BPA vs Control; $ indicates p<0.05 vs Control using Student’s t-test.
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References

    1. Alford FP, Henriksen JE, Rantzau C, Beck-Nielsen H, 2018. Glucose effectiveness is a critical pathogenic factor leading to glucose intolerance and type 2 diabetes: An ignored hypothesis. Diabetes Metab Res Rev 34, e2989. - PubMed
    1. Anderson LM, Riffle L, Wilson R, Travlos GS, Lubomirski MS, Alvord WG, 2006. Preconceptional fasting of fathers alters serum glucose in offspring of mice. Nutrition 22, 327–331. - PubMed
    1. Bansal A, Rashid C, Xin F, Li C, Polyak E, Duemler A, van der Meer T, Stefaniak M, Wajid S, Doliba N, Bartolomei MS, Simmons RA, 2017. Sex- and Dose- Specific Effects of Maternal Bisphenol A Exposure on Pancreatic Islets of First- and Second-Generation Adult Mice Offspring. Environmental health perspectives 125, 097022. - PMC - PubMed
    1. Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL, 2008. Exposure of the U.S. population to bisphenol A and 4-tertiary-octylphenol: 2003–2004. Environmental health perspectives 116, 39–44. - PMC - PubMed
    1. Carwile JL, Michels KB, 2011. Urinary bisphenol A and obesity: NHANES 2003–2006. Environmental research 111, 825–830. - PMC - PubMed
-